PDF(Pubmed)
Abstract：
UNASSIGNED: While an association between femoroacetabular impingement (FAI) and osteoarthritis (OA) has been reported, the mechanistic differences and transition between the 2 conditions is not fully understood. In FAI, cartilage lesions at the femoral head-neck junction can sometimes be visualized during hip arthroscopy.
UNASSIGNED: The purpose of this study was to describe a unique dimpled pattern of superficial fissured cartilage lesions on the femoral head-neck junction at impingement site in patients with FAI syndrome (FAIS) and to evaluate the clinical, histological, and genetic phenotype of this cartilage. We hypothesized that the cartilage lesions may indicate risk for, or predict occurrence of, OA.
UNASSIGNED: Controlled laboratory study.
UNASSIGNED: Six hips (6 patients; mean age, 34.2 ± 12.9 years; range, 19-54 years) with dimpled or fissured cartilage were included among patients who underwent hip arthroscopy for treatment of FAIS from October 2020 through December 2021. This affected cartilage (dimple-pattern group) and normal cartilage (control group) on the femoral head-neck junction were collected from the same patients and evaluated for histological quantification by Mankin scores and expression of proteins related to cartilage degeneration (eg, matrix metalloproteinase [MMP]-1, MMP-2, MMP-3, MMP-10, and MMP-12, tissue inhibitor of metalloproteinase [TIMP]-1 and TMP-2, aggrecan neopepitope CS846, and hyaluronic acid [HA]) with the use of Milliplex Multiplex Assays.
UNASSIGNED: All 6 hips were of the mixed FAI subtype. Preoperatively, 4 of 6 hips had Tönnis grade 1 radiographic changes, which was associated with greater femoral head chondral damage visualized intraoperatively. Mankin scores for the normal cartilage group and the dimple-pattern group were 0.67 ± 0.82 and 3.3 ± 0.82, respectively. Dimple pattern fissured cartilage showed a significant increase in Mankin score (P = .031) and a significant increase in protein expression of CS846 (P = .031) compared with normal cartilage. There were no significant differences in MMPs, TIMPs, or HA levels between the 2 groups.
UNASSIGNED: The dimple pattern fissured cartilage, compared to normal cartilage, showed histologically significant cartilage degeneration and a significant increase in protein expression of CS846, a biomarker for early OA.
UNASSIGNED: This lesion serves as helpful visual indicator of early degeneration of the cartilage of femoral head-neck junction caused by FAIS.
UNASSIGNED: The purpose of this study was to describe a unique dimpled pattern of superficial fissured cartilage lesions on the femoral head-neck junction at impingement site in patients with FAI syndrome (FAIS) and to evaluate the clinical, histological, and genetic phenotype of this cartilage. We hypothesized that the cartilage lesions may indicate risk for, or predict occurrence of, OA.
UNASSIGNED: Controlled laboratory study.
UNASSIGNED: Six hips (6 patients; mean age, 34.2 ± 12.9 years; range, 19-54 years) with dimpled or fissured cartilage were included among patients who underwent hip arthroscopy for treatment of FAIS from October 2020 through December 2021. This affected cartilage (dimple-pattern group) and normal cartilage (control group) on the femoral head-neck junction were collected from the same patients and evaluated for histological quantification by Mankin scores and expression of proteins related to cartilage degeneration (eg, matrix metalloproteinase [MMP]-1, MMP-2, MMP-3, MMP-10, and MMP-12, tissue inhibitor of metalloproteinase [TIMP]-1 and TMP-2, aggrecan neopepitope CS846, and hyaluronic acid [HA]) with the use of Milliplex Multiplex Assays.
UNASSIGNED: All 6 hips were of the mixed FAI subtype. Preoperatively, 4 of 6 hips had Tönnis grade 1 radiographic changes, which was associated with greater femoral head chondral damage visualized intraoperatively. Mankin scores for the normal cartilage group and the dimple-pattern group were 0.67 ± 0.82 and 3.3 ± 0.82, respectively. Dimple pattern fissured cartilage showed a significant increase in Mankin score (P = .031) and a significant increase in protein expression of CS846 (P = .031) compared with normal cartilage. There were no significant differences in MMPs, TIMPs, or HA levels between the 2 groups.
UNASSIGNED: The dimple pattern fissured cartilage, compared to normal cartilage, showed histologically significant cartilage degeneration and a significant increase in protein expression of CS846, a biomarker for early OA.
UNASSIGNED: This lesion serves as helpful visual indicator of early degeneration of the cartilage of femoral head-neck junction caused by FAIS.
摘要：
■虽然已经报道了股骨髋臼撞击（FAI）与骨关节炎（OA）之间的关联，这两种条件之间的机制差异和过渡还没有完全理解。在FAI中,在髋关节镜检查期间，有时可以观察到股骨头-颈交界处的软骨损伤。
■这项研究的目的是描述FAI综合征（FAIS）患者撞击部位股骨头颈交界处浅表裂隙软骨病变的独特凹痕模式，并评估临床，组织学,和这个软骨的遗传表型。我们假设软骨损伤可能表明，或预测的发生，
■对照实验室研究。
■六髋（6名患者；平均年龄，34.2±12.9年；范围，从2020年10月至2021年12月接受髋关节镜检查以治疗FAIS的患者中，包括19-54岁）的软骨凹陷或裂隙。从同一患者中收集股骨头-颈交界处受影响的软骨（酒窝模式组）和正常软骨（对照组），并通过Mankin评分和与软骨变性相关的蛋白质表达来评估组织学定量（例如，基质金属蛋白酶[MMP]-1，MMP-2，MMP-3，MMP-10和MMP-12，金属蛋白酶[TIMP]-1和TMP-2的组织抑制剂，聚集蛋白聚糖新表位CS846和透明质酸[HA]）。
■所有6个臀部均为混合FAI亚型。术前,6个臀部中有4个有Tönnis1级影像学改变，这与术中可视化的较大股骨头软骨损伤有关。正常软骨组和酒窝模式组的Mankin评分分别为0.67±0.82和3.3±0.82。与正常软骨相比，凹陷型裂隙软骨的Mankin评分显着增加（P=.031），CS846蛋白表达显着增加（P=.031）。MMPs没有显著差异,TIMP,或2组之间的HA水平。
■酒窝图案裂开的软骨，与正常软骨相比，显示组织学上明显的软骨退化和CS846蛋白表达的显着增加，CS846是早期OA的生物标志物。
■该病变可作为FAIS引起的股骨头-颈交界处软骨早期退变的有用视觉指标。
■这项研究的目的是描述FAI综合征（FAIS）患者撞击部位股骨头颈交界处浅表裂隙软骨病变的独特凹痕模式，并评估临床，组织学,和这个软骨的遗传表型。我们假设软骨损伤可能表明，或预测的发生，
■对照实验室研究。
■六髋（6名患者；平均年龄，34.2±12.9年；范围，从2020年10月至2021年12月接受髋关节镜检查以治疗FAIS的患者中，包括19-54岁）的软骨凹陷或裂隙。从同一患者中收集股骨头-颈交界处受影响的软骨（酒窝模式组）和正常软骨（对照组），并通过Mankin评分和与软骨变性相关的蛋白质表达来评估组织学定量（例如，基质金属蛋白酶[MMP]-1，MMP-2，MMP-3，MMP-10和MMP-12，金属蛋白酶[TIMP]-1和TMP-2的组织抑制剂，聚集蛋白聚糖新表位CS846和透明质酸[HA]）。
■所有6个臀部均为混合FAI亚型。术前,6个臀部中有4个有Tönnis1级影像学改变，这与术中可视化的较大股骨头软骨损伤有关。正常软骨组和酒窝模式组的Mankin评分分别为0.67±0.82和3.3±0.82。与正常软骨相比，凹陷型裂隙软骨的Mankin评分显着增加（P=.031），CS846蛋白表达显着增加（P=.031）。MMPs没有显著差异,TIMP,或2组之间的HA水平。
■酒窝图案裂开的软骨，与正常软骨相比，显示组织学上明显的软骨退化和CS846蛋白表达的显着增加，CS846是早期OA的生物标志物。
■该病变可作为FAIS引起的股骨头-颈交界处软骨早期退变的有用视觉指标。
